Dyspepsia & Gastroduodenal Ulcer

Gastroduodenal ulceration is a breach of the epithelium that penetrates the muscularis mucosa (of the gastric or duodenal lining).  It must be confirmed endoscopically for the diagnosis to be made.

Epidemiology

  • It has a reported incidence of 1-4/1000, and is much more common in men (particularly duodenal ulcers- 5:1)
  • Incidence has reduced in recent years due to widespread prescription of PPIs, awareness of NSAID use and risk, and eradication of the causal organism, H Pylori, with antibiotic treatment

Aetiology

  • Helicobacter pylori
    • In the western world, the most common site of H pylori infection is the antrum of the stomach
      • In patients from the developing world (particularly Asia) and those with a family history of gastric cancer- a chronic atrophic pangastritis may be caused by H pylori infection affecting the entire stomach
        • This is thought to be due, at least in part, to a difference in H pylori strains
          • The VacA and CagA genes in H pylori are thought to play an important role in carcinogenesis and ulceration (respectively, although CagA may be important in both)
          • Human genetics, e.g. IL1B gene cluster, may also play a role
    • Causes local inflammation resulting in dysfunction of D cells located there.  This causes a reduction in somatostatin production
      • Somatostatin is important in acting on parietal cells in the fundus of the stomach to reduce secretion of gastric acid
      • It also acts to reduce the release of pro-secretory hormones such as gastrin, secretin and histamine (therefore, in an infected state, the levels of these hormones increase)
    • This increases acid causes increased cell turnover in the duodenum, metaplasia and eventually ulceration, particularly in those with other risk factors (it is not certain whether gastric ulcers follow the same pathophysiology)
  • NSAIDs
    • COX-1 inhibition prevent the production of protective prostaglandins, which are important in maintaining the integrity of the gastric wall
    • If there is an underlying H pylori infection, this could precipitate ulceration
  • Smoking
  • Alcohol (alcohol induced gastritis precipitating a peptic ulcer)

Presentation

  • Symptoms may be vague and non-specific
    • Epigastric pain
      • Classically post-prandial with gastric ulcer and 2-3 hours after a meal with duodenal ulcer (hunger-pangs)
      • Epigastric pain may be relieved by food in a duodenal ulcer (often not so with gastric)
      • Often wakens sleep (more common in duodenal)
      • Pain radiating to the back may indicate a complicating pancreatitis (posterior gastric ulcer)
      • May be worsened by fatty foods
    • Nausea
    • Oral flatulence, bloating/distention (may be associated with chronic duodenal ulcer causing stricture/obstruction)
  • There might not be many signs (maybe epigastric tenderness)

What is important is to be able to assess patients for dyspepsia with alarm features e.g.

  • Chronic GI bleeding
  • Unintentional weight loss
  • Progressive dysphagia
  • Persistant vomiting
  • Iron deficiency anaemia
  • Epigastric mass
  • If patients are >55 years with persistent or unexplained recent-onset dyspepsia

fref

Investigation/Management of Dyspepsia

  • For patients with dyspepsia and acute GI bleeding- admit to hospital
  • For patients with dyspepsia and alarm features
    • Arrange urgent endoscopy
    • Stop any NSAIDs and modify any other drugs which may be contributing
    • Advise on lifestyle
      • Lose weight
      • Stop smoking
      • Stop alcohol consumption
      • Stop food that worsens symptoms
    • Prescribe either an alginate e.g. sodium bicarbonate, or an antacid.  DO NOT PRESCRIBE H2 antagonists OR PPIs for at least 2 weeks prior to endoscopy
  • For patients without alarm features
    • FBC- check anaemia
    • Review drugs
    • Prescribe an antacid or an alginate
    • If it is possible to stop any NSAIDs
      • If not possible, consider switching NSAID from aspirin to another NSAID e.g. clopidogrel, plus a PPI
    • For persistent symptoms, either prescribe a PPI (full dose for 1 month) or test and treat for H pylori (NB if the former doesn’t work, test for H pylori anyway)
      • Tests for H pylori
        • Urea breath test or stool antigen test (contraindicated if taken antibiotics in the past four weeks or a PPI in the past 2)
          • The latter is best for re-testing should this be required (e.g. in poor compliance, FHx of gastric cancer, those requiring NSAIDs, severe symptoms etc)
        • Serology may be used if the other tests have failed
      • Treatments for H pylori infection
        • Amoxixillin 1g + Clarithromycin 500mg + either lansoprazole 30mg or omeprazole 20mg for 7 days
        • Clarithromycin 250mg + metronidazole 400mg + either lansoprazole or omeprazole for 7 days
    • If neither treatment for H pylori nor PPI treatment for 1 month works, consider referral or a month trial of either a prokinetic (e.g. domperidone) or an H2-receptor antagonist
  • NB PPI prescriptions for peptic ulcer disease should not be indefinite.  Patients should stop taking the PPI once symptoms have resolved.  If symptoms return, the PPI can be restarted or alternative drugs considered.  In any case, a regular review of patient drugs should be arranged, particularly in patients with polypharmacy.

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